A nuclear lncRNA Linc00839 as a Myc target to promote breast cancer chemoresistance via PI3K/AKT signaling pathway

0301 basic medicine 0303 health sciences Gene Expression Profiling Genes, myc Breast Neoplasms Original Articles Xenograft Model Antitumor Assays 3. Good health Gene Expression Regulation, Neoplastic Disease Models, Animal Mice Phosphatidylinositol 3-Kinases 03 medical and health sciences Drug Resistance, Neoplasm Cell Line, Tumor Animals Humans Female RNA Interference RNA, Long Noncoding Proto-Oncogene Proteins c-akt In Situ Hybridization, Fluorescence Cell Proliferation Signal Transduction
DOI: 10.1111/cas.14555 Publication Date: 2020-07-03T15:38:19Z
ABSTRACT
Abstract Chemoresistance has become a leading cause of mortality in breast cancer patients and is one the major obstacles for improving clinical outcome. Long noncoding RNAs play important roles tumorigenesis chemoresistance. However, involvement regulation lncRNAs chemoresistance are not completely understood. Here, we reported that Linc00839 was localized nucleus upregulated chemoresistant cells tissues, high level associated with poor prognosis. Knockdown significantly suppressed proliferation, invasion, migration, sensitized to paclitaxel vitro inhibited transplant tumor development vivo. Mechanistically, found Myc could directly bind promoter region activate its transcription. Furthermore, overexpression increased expression RNA‐binding protein Lin28B activated PI3K/AKT signaling pathway. We also discovered positively interacted tissues. Taken together, first time, showed by promoted proliferation through binding Lin28B. These findings provide new insight into regulatory mechanism propose Myc/Linc00839/Lin28B feedback loop be used as novel therapeutic target cancer.
SUPPLEMENTAL MATERIAL
Coming soon ....
REFERENCES (44)
CITATIONS (44)